Anaphylaxis By : O. Ahmadi, MD. Professor Assistant of Esfahan medical School, Emergency Department...

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Transcript of Anaphylaxis By : O. Ahmadi, MD. Professor Assistant of Esfahan medical School, Emergency Department...

Anaphylaxis

By : O. Ahmadi, MD. Professor Assistant By : O. Ahmadi, MD. Professor Assistant of Esfahan medical School, Emergency of Esfahan medical School, Emergency

Department of Al-Zahra HospitalDepartment of Al-Zahra Hospital

Case

A child with bee sting came to ED

He has Facial Edema, wheezing VS Stable

Questions

Drugs? Rehydration? Epinephrine Intubation?

Anaphylaxis

Anaphylaxis is a severe, systemic allergic reaction

multisystem involvement, including the skin, airway, vascular system, and GI

Severe cases may result in complete obstruction of the airway, cardiovascular collapse, and death

Anaphylactoid or pseudoanaphylactic reactions display a similar clinical syndrome, but they are not immune-mediated. Treatment for the two conditions is similar

Etiology Pharmacologic agents Antibiotics (especially parenteral

penicillins and other ß-lactams), aspirin and nonsteroidal anti-

inflammatory drugs intravenous (IV) contrast agents are

the most frequent medications associated with life-threatening anaphylaxis.

Latex Much attention has focused on

latex-induced anaphylaxis, but it is actually quite rare. A decade-long registry of anaphylactic deaths in England has not registered any latex-associated deaths

Stinging insects ants, bees, hornets, wasps, and yellow

jackets. Fatal anaphylaxis can develop when a

person with IgE antibodies induced by a previous sting is stung again

A fatal reaction occurs within 10 to 15 minutes. Cardiovascular collapse is the most common mechanism

Foods Peanuts, seafood, and wheat are the

foods most frequently associated with life-threatening anaphylaxis.

Bronchospasm and asphyxia are the most frequent mechanisms

Signs and Symptoms Serious upper airway (laryngeal) edema,

lower airway edema (asthma), or both may develop, causing stridor and wheezing.

Rhinitis

Cardiovascular collapse is the most common periarrest manifestation

Gastrointestinal signs and symptoms of anaphylaxis include abdominal pain, vomiting, and diarrhea

Differential Diagnoses

Scombroid poisoning Angioedema Angiotensin-converting enzyme

(ACE) inhibitors Severe, near-fatal asthma attacks panic disorder

Cardiac Arrest

Aggressive volume expansion High-dose epinephrine IV Antihistamine IV Steroid therapy Asystole/Pulseless Electrical

Activity (PEA) Algorithms Prolonged CPR

Aggressive volume expansion profound vasodilation Increases intravascular capacity Massive volume replacement is

needed. At least 2 large-bore IVs with pressure bags to administer large volume (typically between 4 and 8 L) of isotonic crystalloid as quickly as possible

High-dose epinephrine IV

Use a rapid progression to high dose without hesitation in patients in full cardiac arrest.

A commonly used sequence is 1 to 3 mg IV (3 minutes), 3 to 5 mg IV (3 minutes), then 4 to 10 µg/min infusion

Antihistamine IV. There is little data about the value of antihistamines in anaphylactic cardiac arrest, but it is reasonable to assume that little additional harm could result

Steroid therapy. Steroids given during a cardiac arrest will have little effect, but they may have value in the early hours of any postresuscitation period

Asystole/Pulseless Electrical Activity (PEA) Algorithms. The arrest rhythm in anaphylaxis is often PEA or asystole.

Prolonged CPR. Effective CPR may maintain sufficient oxygen delivery until the catastrophic effects of the anaphylactic reaction resolve.

Interventions to Prevent Cardiopulmonary Arrest

Oxygen. Administer oxygen at high flow rates.

Epinephrine

o Administer epinephrine by IM injection early to all patients with signs of a systemic reaction, especially hypotension, airway swelling, or definite difficulty breathing.

o Use an IM dose of 0.3 to 0.5 mg (1:1000) repeated every 15 to 20 minutes if there is no clinical improvement

Administer IV epinephrine if anaphylaxis appears to be severe with immediate life-threatening manifestations

Use epinephrine (1:10 000) 0.1 mg IV slowly over 5 minutes. Epinephrine may be diluted to a 1:10 000 solution before infusion.

An IV infusion at rates of 1 to 4 µg/min may prevent the need to repeat epinephrine injections frequently

Close monitoring is critical because fatal

overdose of epinephrine has been reported

Patients who are taking ß-blockers have increased incidence and severity of anaphylaxis and can develop a paradoxical response to epinephrine.

Consider glucagon as well as ipratropium for these patients

Aggressive fluid resuscitation. Give isotonic crystalloid (eg, normal saline) if hypotension is present and does not respond rapidly to epinephrine. A rapid infusion of 1 to 2 L or even 4 L may be needed initially

Antihistamines. Administer antihistamines slowly IV or IM (eg, 25 to 50 mg of diphenhydramine)

H2 blockers. Administer H2 blockers such as cimetidine (300 mg orally, IM, or IV)

Provide inhaled albuterol if bronchospasm is a major feature.

Inhaled ipratropium may be especially useful for treatment of bronchospasm in patients receiving ß-blockers.

Note that some patients treated for near-fatal asthma actually had anaphylaxis, so they received repeated doses of conventional bronchodilators rather than epinephrine

Inhaled ß-adrenergic agents

Corticosteroids Infuse high-dose IV corticosteroids early in the course of therapy. Beneficial effects are delayed at least 4 to 6 hours.

Removal of venom sac. Insect envenomation by bees (but not wasps) may leave a venom sac attached to the victim’s skin. At some point during initial assessment, look at the sting site, and if you see a stinger, immediately scrape it or any insect parts at the site of the sting, using the dull edge of a knife.

Avoid compressing or squeezing any insect parts near the skin because squeezing may increase envenomation

Potential Therapies

Vasopressin. There are case reports that vasopressin may benefit severely hypotensive patients.

Atropine. Case reports suggest that when relative or severe bradycardia is present, there may be a role for administration of atropine.

Glucagon. For patients who are unresponsive to epinephrine, especially those receiving ß-blockers, glucagon may be effective. This agent is short-acting; give 1 to 2 mg every 5 minutes IM or IV. Nausea, vomiting, and hyperglycemia are common side effects

Symptoms may recur in some patients (up to 20%) within 1 to 8 hours (biphasic response).

Biphasic responses have been reported to occur up to 36 hours after the initial reaction. A patient who remains symptom-free for 4 hours after treatment may be discharged. Severity of reaction or other problems, however, may necessitate longer periods of observation.

Observation

Airway Obstruction

Early elective intubation is recommended for patients observed to develop hoarseness, lingual edema, stridor, or oropharyngeal swelling.

Patients with angioedema pose a particularly worrisome problem because they are at high risk for rapid deterioration

Patients can deteriorate over a brief period of time ( to 3 hours), with progressive development of stridor, dysphonia or aphonia, laryngeal edema, massive lingual swelling, facial and neck swelling, and hypoxemia. This may occur when patients have a delayed presentation to the hospital or fail to respond to therapy

At this point use of either the laryngeal mask airway or the Combitube will be ineffective, and endotracheal intubation and cricothyrotomy may be difficult or impossible.

Attempts at endotracheal intubation may only further increase laryngeal edema or cause trauma to the airway

Thank You